The effect of acute hypoxia on heat shock protein 72 expression and oxidative stress in vivo.

The inducible human stress protein HSP72 performs vital roles within the body at rest and during periods of stress. Recently, a previously disclosed quadratic trend in basal HSP72 expression was shown to be reliable and repeatable. The notion of a physiological stressor such as hypoxia disrupting this basal quadratic trend is an interesting one. Monocyte-expressed HSP72 and TBARS were determined every 3 h, over a 12-h period in 12 healthy male subjects on two separate days, with trial day one ascertaining control values. A hypoxic intervention consisting of 75 min at a simulated altitude of 2,980 m, commencing and ceasing at 0930 and 1045, respectively, was incorporated on trail day 2. The hypoxic condition induced significantly (elevated) HSP72 values at 1100 (P = 0.002), 1400 (P < 0.001), 1700 (P = 0.034) and 2000 (P = 0.041) compared to control. Significant increases in plasma TBARS were seen in the hypoxic condition compared to control at 1100 (P = 0.006) and 1400 (P = 0.032). The results demonstrate that a 75-min bout of normobaric hypoxia is sufficient to induce significant increases in HSP72 expression, which disrupts the basal quadratic trend shown by others and here in the control condition. This increase may be linked to the observed changes in oxidative stress. These results may provide a tool for manipulating basal monocyte HSP72 expression within human heat acclimation exercise protocols.